CONTROL OF APETITE METABOLISM GH Glucose Homeostasis GLYCOGENOLYSIS

CONTROL OF APETITE & METABOLISM

GH Glucose Homeostasis GLYCOGENOLYSIS GLUCONEOGENESIS LIVER & MUSCLE GLUCAGON ISLET -CELLS CORTISONE & EPINEPHRINE MEALS SERUM GLUCOSE NORMAL SERUM GLUCOSE 80 -120 mg/dl ISLET -CELLS INSULIN LIVER & MUSCLE SERUM GLUCOSE UPTAKE METABOLIC DEMANDS

HYPOTHALAMUS: ARCUATE NUCLEUS • ANTERIOR PITUITARY RELEASING HORMONES • ENERGY RESERVES AND METABOLISM – OREXIGENIC/ANOREXIGENIC NEURONS – INCREASE/DECREASE METABOLISM – RECEPTORS FOR PERIPHERAL SIGNALS

ARCUATE NUCLEUS • TWO TYPES OF NEURONS • MELANOCORTIN – – POMC αMSH INHIBITS FEEDING BEHAVIOR INCREASES METABOLISM • NEUROPEPTIDE-Y (NPY) – NPY – AGOUTI-RELATED PEPTIDE (Ag. RP) • COMPETITIVE INHIBITOR OF MELANOCORTIN RECEPTORS – STIMULATES FEEDING BEHAVIOR – DECREASES METABOLISM – INHIBITS MELANOCORTIN NEURONS

ARCUATE NUCLEUS FEEDING BEHAVIOR (+) NPY (-) METABOLIC RATE (-) (+) (-) ARCUATE NUCLEUS αMSH

ENERGY BALANCE INDICATORS • LONG-TERM ENERGY STORES (ADIPOSE) – LEPTIN – INSULIN • SHORT-TERM ENERGY STORES (SATIETY) – GHRELIN – PEPTIDE YY – CHOLECYSTOKININ (CCK) – GLP-1

Leptin • Produced by fat cells – Level of leptin produced is directly related to how much fat is in the fat cell. • Peptide • Anorexogenic • Increases metabolism

Leptin Deficiency

ARCUATE NUCLEUS FEEDING BEHAVIOR (+) (-) METABOLIC RATE (-) (+) (-) NPY αMSH ARCUATE NUCLEUS GHRELIN LEPTIN INSULIN PEPTIDE YY CCK GLP-1(? )

CONTROL OF FOOD INTAKE AND METABOLISM CCK